| First Author | Kim J | Year | 2015 |
| Journal | Biochim Biophys Acta | Volume | 1853 |
| Issue | 2 | Pages | 500-12 |
| PubMed ID | 25499765 | Mgi Jnum | J:234463 |
| Mgi Id | MGI:5790040 | Doi | 10.1016/j.bbamcr.2014.12.003 |
| Citation | Kim J, et al. (2015) Prostaglandin F2alpha receptor (FP) signaling regulates Bmp signaling and promotes chondrocyte differentiation. Biochim Biophys Acta 1853(2):500-12 |
| abstractText | Prostaglandins are a group of lipid signaling molecules involved in various physiological processes. In addition, prostaglandins have been implicated in the development and progression of diseases including cancer, cardiovascular disease, and arthritis. Prostaglandins exert their effects through the activation of specific G protein-coupled receptors (GPCRs). In this report, we examined the role of prostaglandin F2alpha receptor (FP) signaling as a regulator of chondrocyte differentiation. We found that FP expression was dramatically induced during the differentiation of chondrocytes and was up-regulated in cartilages. Forced expression of FP in ATDC5 chondrogenic cell line resulted in the increased expression of differentiation-related genes and increased synthesis of the extracellular matrix (ECM) regardless of the presence of insulin. Similarly, PGF2alpha treatment induced the expression of chondrogenic marker genes. In contrast, knockdown of endogenous FP expression suppressed the expression of chondrocyte marker genes and ECM synthesis. Organ culture of cartilage rudiments revealed that PGF2alpha induces chondrocyte hypertrophy. Additionally, FP overexpression increased the levels of Bmp-6, phospho-Smad1/5, and Bmpr1a, while knockdown of FP reduced expression of those genes. These results demonstrate that up-regulation of FP expression plays an important role in chondrocyte differentiation and modulates Bmp signaling. |
